Hyperprolactinemia and Impaired Pituitary Response to Suppression and Stimulation in Chronic Renal Failure: Reversal after Transplantation*

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Abstract
PRL secretion was evaluated in 18 patients with chronic renal failure (CRF) and 8 renal transplant (RT) recipients and was compared with that in 33 controls. Basal PRL levels (nanograms per ml; mean ± SEM) of 34 ± 4 in CRF patients were 3 and 2 times higher than in controls and RT patients [12 ± 1 (P < 0.001) and 16 ± 3 (P < 0.01), respectively]. Plasma PRL values 2 SDS or greater than control were present in 77% of CRF patients. After 0.5 g L-dopa orally, plasma PRL was suppressed by 16 ± 3% in CRF patients as compared to 57 ± 4% and 44 ± 8%, respectively, in controls (P < 0.001) and RT subjects (P < 0.01). During dopamine infusion (4 /ig/kg-min), the maximal fall of plasma PRL in CRF patients was 20 ± 3%. In contrast, the decrement of PRL in normal subjects was 46 ± 6% (P < 0.001) and in the RT recipients was 48 ± 8% (P < 0.001). After 500 jug TRH iv, plasma PRL in CRF patients increased by 54 ± 10% at 30 min. The increases of plasma PRL in control and RT subjects were 259 ± 43% (P < 0.001) and 179 ± 51% (P < 0.05), respectively, and occurred more rapidly (at 15 min). The lack of PRL responsiveness to suppressive as well as stimulatory agents suggests a primary pituitary disorder involving either receptor binding or postreceptor phenomena, although the presence of a concomitant defect either in the hypothalamus or elsewhere in the central nervous system cannot be excluded. These disturbances seem to be reversible, as renal transplantation not only corrects the hyperprolactinemia but also restores the responsiveness of the lactotropes to both suppressive and stimulatory agents.

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